Survival of mice bearing orthotopic glioma

Where it participates (unsigned role)

1. Comparing therapeutic efficacy against GL261 orthotopic tumours, mebendazole showed a significant increase in animal survival time whereas vincristine, even at a dose close to its maximum tolerated dose, failed to show any efficacy; vincristine does not penetrate well into brain tumour tissue and displays dose-limiting toxicities including peripheral neuropathy.

   Mebendazole → Vincristine source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"}

   experimental_model

   Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine

   exposure

   Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours

   limitations

   Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do.

   nutrient_topic

   Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

   organism

   Mouse

   plain_language

   Against brain tumours in mice it beat the microtubule drug already in clinical use, which cannot get into the brain.

   primary_references

   [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011

   tissue_or_cell_type

   Glioblastoma

   Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 511–522

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine · source_derived_draft · unverified_draft

   ### mbz-beats-vincristine Comparing therapeutic efficacy against GL261 orthotopic tumours, mebendazole showed a significant increase in animal survival time whereas vincristine, even at a dose close to its maximum tolerated dose, failed to show any efficacy; vincristine does not penetrate well into brain tumour tissue and displays dose-limiting toxicities including peripheral neuropathy. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: Against brain tumours in mice it beat the microtubule drug already in clinical use, which cannot get into the brain. organism: Mouse tissue_or_cell_type: Glioblastoma experimental_model: Concentration-matched comparison of viability, microtubule polymerisation and metaphase arrest, with NCI COMPARE analysis and a head-to-head animal comparison against vincristine limitations: Tests whether the anticancer effect is the microtubule effect by matching concentrations across three assays, which most repurposing studies do not do. exposure: Mebendazole against vincristine close to its maximum tolerated dose in orthotopic GL261 tumours evidence_span: {"source_cache": "artifacts/mebendazole-research/28386621.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865", "start_char": 0, "end_char": 1788, "text_sha256": "20ef610d6b4a341f8a0a3f731bbea5477badbee517062c303bbf1075f3a29865"} [mbz-p28386621] Repurposing Mebendazole as a Replacement for Vincristine for the Treatment of Brain Tumors. (2017). https://pubmed.ncbi.nlm.nih.gov/28386621/ DOI: 10.2119/molmed.2017.00011

   Complete structured claim and evidence

2. In glioblastoma cell lines mebendazole displayed cytotoxicity with half-maximal inhibitory concentrations ranging from 0.1 to 0.3 micromolar, disrupted microtubule formation in those cells with in vitro activity correlated with reduced tubulin polymerization, and significantly extended mean survival by up to 63% in syngeneic and xenograft orthotopic mouse glioma models; the programme began with the serendipitous observation that fenbendazole, used to treat pinworm infection, inhibited brain tumour engraftment.

   Mebendazole → Viability of glioblastoma cells source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/mebendazole-research/21764822.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6", "start_char": 0, "end_char": 1210, "text_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6"}

   experimental_model

   Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models

   exposure

   Mebendazole compared with fenbendazole, at doses documented as safe in humans

   limitations

   The observation that started the programme was serendipitous, from pinworm treatment of laboratory animals. Mouse models, and the survival gain is a mean rather than a cure.

   nutrient_topic

   Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

   organism

   Human cells and mouse

   plain_language

   The worm drug killed brain tumour cells at low concentrations and let mice live substantially longer.

   primary_references

   [mbz-p21764822] Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. (2011). https://pubmed.ncbi.nlm.nih.gov/21764822/ DOI: 10.1093/neuonc/nor077

   tissue_or_cell_type

   Glioblastoma

   Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 485–496

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models · source_derived_draft · unverified_draft

   ### mbz-glioma-cytotoxicity In glioblastoma cell lines mebendazole displayed cytotoxicity with half-maximal inhibitory concentrations ranging from 0.1 to 0.3 micromolar, disrupted microtubule formation in those cells with in vitro activity correlated with reduced tubulin polymerization, and significantly extended mean survival by up to 63% in syngeneic and xenograft orthotopic mouse glioma models; the programme began with the serendipitous observation that fenbendazole, used to treat pinworm infection, inhibited brain tumour engraftment. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: The worm drug killed brain tumour cells at low concentrations and let mice live substantially longer. organism: Human cells and mouse tissue_or_cell_type: Glioblastoma experimental_model: Cell line cytotoxicity, tubulin polymerisation and syngeneic and xenograft orthotopic mouse glioma models limitations: The observation that started the programme was serendipitous, from pinworm treatment of laboratory animals. Mouse models, and the survival gain is a mean rather than a cure. exposure: Mebendazole compared with fenbendazole, at doses documented as safe in humans evidence_span: {"source_cache": "artifacts/mebendazole-research/21764822.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6", "start_char": 0, "end_char": 1210, "text_sha256": "31b328d5c2340f7a4e9b6a3b3d46c68a8c0265c50d483375bc6dc15bb1696ad6"} [mbz-p21764822] Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. (2011). https://pubmed.ncbi.nlm.nih.gov/21764822/ DOI: 10.1093/neuonc/nor077

   Complete structured claim and evidence

3. Polymorph B and polymorph C both increased survival in a GL261 glioma model with B exhibiting greater toxicity, polymorph A showed no benefit, B and C both reached brain concentrations exceeding the GL261 half-maximal inhibitory concentration 29-fold, polymorph C demonstrated a 24-hour brain-to-plasma area-under-curve ratio of 0.82 while B showed higher plasma exposure and a lower ratio, polymorph A presented markedly lower levels in both plasma and brain, and combination with elacridar significantly improved the efficacy of polymorph C in glioma and medulloblastoma models.

   Mebendazole polymorph C → Brain to plasma exposure ratio source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   biomarker_context Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/mebendazole-research/25862759.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3", "start_char": 0, "end_char": 1682, "text_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3"}

   experimental_model

   Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics

   exposure

   Polymorphs A, B and C, alone and with the transporter inhibitor elacridar

   limitations

   Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy.

   nutrient_topic

   Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

   organism

   Mouse

   plain_language

   The same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely.

   primary_references

   [mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681

   tissue_or_cell_type

   Brain and plasma

   trigger_kind

   biomarker_context Imported condition classification; unverified.

   Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 524–535

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics · source_derived_draft · unverified_draft

   ### mbz-polymorph-decides-brain-levels Polymorph B and polymorph C both increased survival in a GL261 glioma model with B exhibiting greater toxicity, polymorph A showed no benefit, B and C both reached brain concentrations exceeding the GL261 half-maximal inhibitory concentration 29-fold, polymorph C demonstrated a 24-hour brain-to-plasma area-under-curve ratio of 0.82 while B showed higher plasma exposure and a lower ratio, polymorph A presented markedly lower levels in both plasma and brain, and combination with elacridar significantly improved the efficacy of polymorph C in glioma and medulloblastoma models. Condition category: biomarker_context nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: The same crystal form that works against worms is the one that gets into the brain; the inert form stays out of the blood entirely. organism: Mouse tissue_or_cell_type: Brain and plasma experimental_model: Polymorph content of marketed and custom tablets measured by infrared spectroscopy, then tested in orthotopic mouse glioma and medulloblastoma models with LC/MS pharmacokinetics limitations: Carries the polymorph distinction across from the anthelmintic use into the oncology use and finds it decides brain exposure. Mouse models, and elacridar is an experimental tool rather than a co-therapy. exposure: Polymorphs A, B and C, alone and with the transporter inhibitor elacridar evidence_span: {"source_cache": "artifacts/mebendazole-research/25862759.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3", "start_char": 0, "end_char": 1682, "text_sha256": "7545a89b4d17461bbe2d8ac8c7f3093b6ae0ce2f20307ab57b524d91f4f827c3"} [mbz-p25862759] Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. (2015). https://pubmed.ncbi.nlm.nih.gov/25862759/ DOI: 10.1158/1078-0432.ccr-14-2681

   Complete structured claim and evidence